Related Experiment Video
Updated: Jul 16, 2025

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
Published on: January 7, 2019
DUSP1 regulates the JAK2/STAT3 signaling pathway through targeting miR-21 in cervical cancer cells
Hailin Chen1, Songsen Ren2, Hui Wan3
1Department of Obstetrics and Gynecology, Qingpu Branch, Zhongshan Hospital Affiliated to Fudan University, Shanghai 201700, China. Shmiky001@126.com.
Abstract:
This study was to investigate the effect of DUSP1 on cervical cancer (CC) cells by targeting the miR-21 regulatory JAK2/STAT3 signaling pathway. For this purpose, fifteen CC patients treated at our hospital from January 2021 to February 2023 were selected. CC tissues and para-cancerous (PC) tissues were collected from the patients, and DUSP1 protein and mRNA expression levels were detected by Western blot and qPCR. The C33a control group (COG) and DUSP1 overexpression group (OVG) were set up: human cervical squamous carcinoma cells (CSCC) in the C33a COG were cultured without any treatment, while the DUSP1 OVG was cultured using DUSP1 gene overexpression lentivirus infection progeny. The proliferation ability of the three groups of cells was measured by CCK8, protein and mRNA expression by Western blot and qPCR, and cell migration and invasion ability by Transwell. It was found that DUSP1 protein and mRNA in CC tissues were reduced compared with those in PC tissues (P<0.05). The miR-21 in the DUSP1 OVG was reduced than those in the C33a COG (P<0.05). The expression of JAK2, STAT3 mRNA and protein in the DUSP1 OVG were reduced compared with those in the C33a COG (P<0.05). In conclusion, overexpression of DUSP1 can target and reduce the expression of miR-21, block the JAK2/STAT3 signaling pathway, reduce the viability of CC cells, inhibit the proliferation and migration and invasion ability of CC cells, and induce apoptosis of CC cells, thus providing a theoretical basis for the targeted treatment of clinical CC.
Insights
Overexpressing DUSP1 in cervical cancer (CC) cells reduces miR-21, inhibiting the JAK2/STAT3 pathway. This suppressed tumor growth, migration, and invasion, offering a potential CC treatment strategy.
Area of Science:
- Oncology
- Molecular Biology
- Signaling Pathways
Background:
- Cervical cancer (CC) remains a significant global health challenge.
- Dysregulation of the JAK2/STAT3 signaling pathway is implicated in CC progression.
- The role of Dual Specificity Phosphatase 1 (DUSP1) in CC requires further elucidation.
Purpose of the Study:
- To investigate the therapeutic potential of DUSP1 in cervical cancer.
- To determine if DUSP1 targets the miR-21 regulatory JAK2/STAT3 signaling pathway in CC cells.
Main Methods:
- Analysis of DUSP1 and miR-21 expression in CC tissues and cell lines.
- Establishment of a DUSP1 overexpression model in human cervical squamous carcinoma cells (CSCC).
- Assessment of cell proliferation, migration, invasion, and apoptosis using CCK8, Transwell assays, Western blot, and qPCR.
Main Results:
- DUSP1 expression was significantly reduced in CC tissues compared to para-cancerous tissues.
- Overexpression of DUSP1 led to decreased miR-21 levels.
- DUSP1 overexpression suppressed JAK2 and STAT3 expression, inhibiting cell proliferation, migration, and invasion.
Conclusions:
- DUSP1 functions as a tumor suppressor in cervical cancer.
- Overexpression of DUSP1 effectively inhibits CC cell viability and progression by targeting the miR-21/JAK2/STAT3 pathway.
- DUSP1 represents a promising therapeutic target for cervical cancer treatment.
Related Concept Videos
The JAK-STAT Signaling Pathway
Abnormal Proliferation
Inhibition of Cdk Activity
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...

